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C Decoster

Publications and source records attributed to C Decoster.

16 recordsLinked to original sources
PubMed1991

Neuroendocrine rhythms and sleep in aging men.

To delineate the physiological effects of aging on basal levels and temporal patterns of neuroendocrine secretions, the 24-h profiles of cortisol, thyroid-stimulating hormone (TSH), melatonin, prolactin, and growth hormone (GH) levels were simultaneously obtained at frequent intervals in eight healthy, active elderly men, age 67-84 yr and in eight young male adults, age 20-27 yr. The study was preceded by an extended period of habituation to laboratory conditions, and sleep was polygraphically recorded. Mean cortisol levels in the elderly were normal, but the amplitude of the circadian rhythm was reduced. Circulating levels of daytime and nighttime levels of both TSH and GH were greatly diminished in old age. In contrast, prolactin and melatonin concentrations were decreased during the nighttime only. The circadian rises of cortisol, TSH, and melatonin occurred 1-1.5 h earlier in elderly subjects, and the distribution of rapid-eye-movement stages during sleep was similarly advanced, suggesting that circadian timekeeping is modified during normal senescence. Despite perturbations of sleep, sleep-related release of GH and prolactin occurred in all elderly men. Age-related decreases in hormonal levels were associated with a decrease in the amplitude, but not the frequency, of secretory pulses. These findings demonstrate that the normal process of aging involves alterations in the central mechanisms controlling the temporal organization of endocrine release in addition to a reduction of secretory outputs.

Adult↗
PubMed1989

Decreased basal and stimulated thyrotropin secretion in healthy elderly men.

To delineate the effects of aging on basal and stimulated TSH secretion, we studied the 24-h profile of plasma TSH levels and the TSH response to TRH stimulation (200 micrograms TRH, iv) in eight healthy elderly men, aged 67-84 yr, and eight normal young men, aged 20-27 yr. Subjects with thyroid antibodies against microsomal or thyroglobulin antigens were excluded. During the 24-h study, blood was sampled at 15-min intervals. TSH levels were measured by an ultrasensitive immunoradiometric assay. Sleep was polygraphically monitored, and circadian and pulsatile TSH variations were quantified using specifically designed computer algorithms. In older men, the 24-h mean TSH concentration was approximately 50% lower than that in young men (0.78 +/- 0.37 vs. 1.43 +/- 0.41 microU/mL; P less than 0.01), but basal T3 levels were only slightly lower (93 +/- 12 vs. 115 +/- 16 ng/dL; P less than 0.02), while basal T4 levels were normal. The normal diurnal variation of TSH levels, with a nocturnal acrophase and an afternoon nadir, as well as the pulsatile nature of TSH release were preserved in elderly men. When expressed in microunits per mL, the amplitude of these temporal variations was reduced in elderly men compared to that in younger subjects. However, when expressed in relation to the mean TSH levels, the amplitudes of diurnal and pulsatile variations were similar in both groups of subjects. TRH-induced TSH secretion was lower in old than in young men (area under the curve, 15.9 +/- 6.3 microU/mL.10 min in elderly men vs. 42.0 +/- 16.6 microU/mL.10 min in young men; P less than 0.002). However, the TRH-induced elevations of T3 and T4 were of similar magnitude in both groups. These results indicate that in healthy elderly men, the overall 24-h TSH secretion is decreased, and the pituitary is less responsive to stimulation by TRH. However, the chronobiological modulation is preserved. These alterations could reflect an adaptative mechanism to the reduced need for thyroid hormones in old age. The thyroid keeps an intact capacity to respond to acute increases in TSH concentrations.

Adult↗
PubMed1989

Nocturnal decrease in glucose tolerance during constant glucose infusion.

Studies comparing glucose tolerance in the morning vs. that in the evening have suggested that time of day may influence glucose regulation. To examine the variation in glucose tolerance throughout the 24-h span, normal subjects were given an iv glucose infusion at a constant rate of either 5 or 8 g/kg.24 h during 30 h, and plasma levels of insulin and glucose were measured at 15-min intervals for the last 24 h of the infusion. The timing of initiation of the infusion was varied to differentiate effects of time of day from effects of duration of the infusion. A nocturnal elevation of glucose levels, culminating around midsleep and corresponding to an increase of about 15% above daytime levels, was observed in all subjects. The timing of this nocturnal maximum was not dependent on the rate of the infusion or on the time elapsed since the beginning of the infusion. Insulin levels did not show a consistent diurnal pattern. Both insulin and glucose exhibited large ultradian oscillations recurring at 100- to 150-min intervals. The amplitude of these oscillations increased with the rate of glucose infusion. These ultradian oscillations of glucose and insulin levels were temporally correlated, with a tendency for glucose pulses to lead insulin pulses by 15-30 min. These results demonstrate in normal subjects the existence of a diurnal variation in glucose tolerance distinct from the dawn phenomenon observed in diabetic subjects and indicate that spontaneous 100- to 150-min oscillations in peripheral glucose and insulin levels characterize stimulated pancreatic function, with the amplitude of the oscillations being dependent on the size of the stimulus.

Activity Cycles↗
PubMed1987

Effect of amiodarone on serum T4 and T3 levels in hyperthyroid patients treated with methimazole.

We investigated the course of thyroid hormones levels in the serum of hyperthyroid patients acutely treated with amiodarone. Ten patients were treated either with amiodarone, 3 X 400 mg daily for 3 days in addition to methimazole, 3 X 20 mg daily for 10 days (Group I; n = 5) or with a placebo plus methimazole at the same doses (Group II; n = 5). Basal T3, T4 and rT3 serum concentrations were: 297 ng/dl, 16.6 micrograms/dl and 507 pg/dl, respectively in Group I and 377 ng/dl, 17.6 micrograms/dl and 362 pg/dl in Group II (NS). Compared with basal values, the drop in serum T3 concentration became significant on Day 1 in Group I, but not until day 5 in Group II. The decrease in serum T3 concentration was significantly higher in Group I than in Group II from Day 1 to Day 7. In Group I, T4 concentration was significantly lower on Days 2, 4 and 6; the percentage drop in T4 calculated from the areas under the curves was higher and the T3/T4 ratio lower on Days 3-5, 7 and 9; rT3 was higher on Days 4 and 5 and its rise was significant on Days 1, 3 and 4. During the follow-up period a transient rise in T4 and T3 concentrations was observed in two patients in Group I when the methimazole dosage was tapered or stopped because of agranulocytosis. In conclusion, in our hyperthyroid patients, amiodarone in conjunction with methimazole induced a greater fall in T3 and T4 than did methimazole alone.

Adult↗
PubMed1987

Tumor promoters as probes of protein kinase C in dog thyroid cell: inhibition of the primary effects of carbamylocholine and reproduction of some distal effects.

The acute effects of phorbol esters, used as probes of protein kinase C activation, were studied on dog thyroid slices incubated in vitro. The derivatives used were: tetradecanoylphorbol acetate (TPA), phorbol-12,13, didecanoate (PDD), phorbol-12,13-diacetate (PDA), and phorbol dibutyrate (PDBu) and as inactive controls, phorbol itself, phorbol-12, myristate and phorbol-13, acetate, in concentrations ranging from 5.10(-8) to 5.10(-6) mol/L. The active phorbol esters had no effect on basal cyclic AMP concentrations; they inhibited cyclic AMP accumulation induced by prostaglandin E1 but not that induced by thyrotropin (TSH) 1 mU/mL and forskolin 10 mumol/L. Phorbol esters like carbamylcholine acutely stimulated iodide organification and inhibited the stimulation of hormone secretion resulting from TSH, Cholera Toxin, forskolin, and Bu2-cyclic AMP action. These metabolic effects did not require the presence of extracellular Ca++, and could not be antagonized by Ca++ depletion or manganese addition. The active phorbol esters abolished the cyclic AMP independent increased PI turnover induced by TSH 10 mU/mL or carbamylcholine (Cchol) 10(-6) mol/L but did not affect the basal incorporation of 32P into phosphatidylinositol. They reduced the 45Ca efflux from preloaded slices below basal levels and blocked the increased 45Ca release induced by TSH and Cchol. They also inhibited the increase in cyclic GMP concentrations resulting from Cchol action but not the effect of the ionophore A23187 (10(-5) mol/L) nor the basal levels of cyclic GMP.(ABSTRACT TRUNCATED AT 250 WORDS)

Alprostadil↗
PubMed1986

Absence of human chorionic somatomammotropin during pregnancy associated with two types of gene deletion.

Complete absence of human somatomammotropin (hCS) was demonstrated in two patients experiencing an otherwise uneventful pregnancy. After delivery, DNA was prepared from the neonate blood or from the placenta and the integrity of the hCS-hGH gene cluster was investigated by Southern blotting and hybridization with an hCS cDNA probe. Patient 1 was found to be homozygous for a deletion involving hCS-A, hGH-V, and hCS-B. Patient 2 was a double heterozygote, with one chromosome bearing the same deletion as that of patient 1, while in the other, only the hCS-A gene was missing. Considerations relative to the frequency of the defect are derived from the present results.

Chromosome Deletion↗
PubMed1985

Negative regulation of cyclic-AMP levels by carbamylcholine in dog thyroid is not mediated by cyclic-GMP.

Carbamylcholine, through calcium, enhances cyclic-GMP accumulation and depresses cyclic-AMP accumulation in TSH stimulated dog thyroid. The results presented show that compounds which can be transformed to nitric oxide increase cyclic-GMP accumulation in the dog thyroid. These compounds do not require extracellular calcium for their action. In thyroid stimulated by TSH, these compounds do not depress AMP accumulation. Cyclic-GMP is not the main intracellular signal involved in the negative regulation of cyclic-AMP levels in dog thyroid.

Animals↗
PubMed1979

Effects of carbamylcholine and ionophore A-23187 on cyclic 3',5'-AMP and cyclic 3',5'-GMP accumulation in dog-thyroid slices.

Carbamylcholine and acetylcholine through a muscarinic type of receptor, KCl, ionophore A-23187 and NaF increased cyclic GMP accumulation in dog-thyroid slices. These effects were abolished in calcium-depleted slices, which findings confirm that Ca2+ is required for cyclic GMP accumulation. All these agents depressed the accumulation of cyclic AMP in TSH-stimulated slices. KCl and NaF depressed cyclic AMP accumulation in TSH-treated slices even when they had been depleted of Ca2+. This suggests a cyclic GMP- and Ca2+-independent mechanism. The absence of inhibition of the effects of the ionophore, NaF and KCl in the presence of atropine suggests that these drugs do not act by inducing the release of acetylcholine in the slices. The effects of carbamylcholine and ionophore A-23187 on cyclic GMP accumulation and protein iodination were reversible; the inhibitions of TSH-induced cyclic AMP accumulation and secretion were non-competitive and were not accompanied by a depression of ATP levels. All these effects were greatly decreased in the absence of extracellular Ca2+. These data suggest that carbamylcholine and ionophore A-23187 act mainly by increasing the influx of extracellular Ca2+ in thyroid cells. However, the persistence of some carbamylcholine effect in the absence of Ca2+ in the medium suggests that this agent may also trigger the release of Ca2+ from an intrafollicular pool. The kinetics of action of carbamylcholine are compatible with a role of cyclic GMP in the inhibition of cyclic AMP accumulation. However, with the ionophore, the depression of cyclic AMP accumulation was much longer than the rise of cyclic GMP, which suggests a mechanism independent of cyclic GMP.

Adenosine Triphosphate↗
PubMed1978

[Calcium, cGMP and cAMP roles in thyroid regulation (author's transl)].

Cholinergic agents induce an accumulation of cGMP in thyroid tissue and inhibit cAMP accumulation and thyroid hormone secretion resulting from TSH action. The aim of the present work was to determine the respective roles of Ca++ and/or cGMP in these actions. The results show that two complementary mechanisms may be demonstrated: 1) cGMP activates phosphodiesterase activity and cAMP hydrolysis. 2) Independently of cyclic nucleotide concentrations, increased intracytoplasmic Ca++ directly inhibits TSH induced stimulated hormone secretion.

Animals↗